Induction Drugs (Ketamine) (Ex2) Flashcards
What type of drug is ketamine?
What type of anesthesia does it produce?
What two properties does it possess?
- Phenycyclidine derivative; NMDA receptor antagonist (PCP; “angel dust”)
- Dissociative anesthesia (psychedelic)
- Amnestic & intense analgesia
What signs and symptoms does dissociative anesthesia (ketamine) produce?
“Zonked” state
- Non-communicative but awake
- Hypertonus & purposeful movements
- Eyes open but “no one’s home”.
What are ketamine’s two greatest advantages over propofol or etomidate?
- No pain at injection (no propylene glycol)
- Profound analgesia at sub-anesthetic doses.
What are the two greatest disadvantages of ketamine?
- Emergence delirium
- Abuse potential
What is Benzethonium Chloride? What is it’s relevance?
- Ketamine preservative that inhibits ACh receptors
Differentiate S(+)Ketamine vs R(-)Ketamine.
S-Ketamine (left-handed isomer) is essentially better.
- More intense analgesia
- ↑metabolism & recovery
- Less salivation
- Lower emergence delirium
What benefits does a racemic ketamine mixture offer?
- Less fatigue & cognitive impairment
- Inhibits catecholamine reuptake at nerve endings (like cocaine).
What is Ketamine’s main mechanism of action?
- Non-competitive inhibition of NMDA (N-methyl-D-aspartate) receptors and inhibits pre-synaptic release of glutamate.
What are Ketamine’s secondary receptor sites?
- Weak GABAA effects.
- Opioid (μ, δ, and κ)
What is Ketamine’s time of onset? (IV & IM)
When would this drug be utilized IM?
- IV: 1 min
- IM: 5 min (mostly for pediatric patients)
What is Ketamine’s duration of action?
What about its lipid solubility?
What is the result of this?
- 10-20 min
- Highly lipid soluble (5-10x greater than thiopental).
- Results: Brain → non plasma bound → peripheral tissue.
What is the Vd and E½ time of ketamine?
- Vd = 3L/kg
- E ½ = 2-3 hours
Name the pharmacokinetic profile of ketamine:
- Clearance:
- Metabolism:
- Excretion:
- Clearance: high hepatic clearance (1L/min)
- Metabolism: CYP450’s.
- Excretion: kidneys
What is the primary metabolite of ketamine and what its its significance?
Norketamine is metabolite (⅓ potency and prolongs analgesia).
In what patient population is ketamine tolerance most often seen?
Burn patients
What is the induction dose of ketamine IV?
What if it is given IM?
- 0.5 - 1.5 mg/kg IV
- 4 - 8 mg/kg IM
What is the maintenance dosing of ketamine?
- 0.2 - 0.5 mg/kg IV
- 4 - 8 mg/kg IM
What is the subanesthetic/analgesic dose of ketamine?
- 0.2 - 0.5 mg/kg IV
What is the post-operative sedation and analgesia dosing for ketamine in pediatric cardiac surgery cases?
1-2 mg/kg/hour
What is the neuraxial epidural analgesia dosing of ketamine?
What about intrathecal route?
- 30mg epidural
- 5 - 50 mg via intrathecal/spinal/subarachnoid
Ketamine is a potent sialagogue. What does this mean for your clinical practice?
- Manage excessive secretions during intubation & watch for coughing/laryngospasm.
What drug and dosing should be used to treat excessive salivary secretions from ketamine administration?
Glycopyrrolate: 0.2mg
You gave ketamine and the patient fell asleep within 30 seconds. If you gave no more doses when would you expect the patient to:
- Wake up?
- Be fully conscious?
- Start remembering things?
- Wake up in 10-20 minutes
- Full consciousness in 60 - 90 min
- Amnestic effects should also wear off in 60 - 90 min.
What patient populations is ketamine best used for?
- Acutely hypovolemic patients
- Asthmatics
- Mental health patients
When would you do an IM induction of a patient?
- Uncooperative and difficult-to-manage mentally challenged patients.
Though ketamine has many indications, when should it be avoided?
- Patients with pulmonary HTN and ↑ICP.
What are Ketamine’s effects on ICP? Why?
- ↑ICP via ↑CBF by 60%
- Potent cerebral vasodilator.
At what dosing will the ICP increasing effects of ketamine plateau?
- 2mg/kg IV
Due to ketamine’s increased excitatory EEG activity, how much does seizure potential increase with administration?
Trick question. No increase in seizure potential with ketamine.
What does the cardiovascular profile of ketamine look like?
How can this side effect profile be blunted?
- SNS stimulation ( ↑ in sBP, PAP, HR, CO, etc.)
- Blunted via pre-med with benzo’s, volatiles, or nitrous.
Say you just gave ketamine and you have an unexpected drop in systolic BP and CO. What happened? How do you treat it?
- Depleted catecholamine stores
- Treat with direct-acting SNS agents (ex. phenylephrine) vs indirect (ex. ephedrine).
What is the Pulmonary profile of ketamine?
- No depression of ventilation with CO₂ response maintained.
- ↑ salivary excretion
- Intact upper airway tone & reflexes.
- Bronchodilator with no histamine release.
What does emergence delirium present like with ketamine?
- Visual, auditory, proprioceptive illusions. Morbid & vivid dreams up to 24 hours.
What is the proposed physiologic mechanism of action for emergence delirium occurrence with ketamine?
Depression of inferior colliculus & medial geniculate nucleus.
What percentage of patients will develop ketamine induced emergence delirium?
How can it be prevented?
- Psychedelic effects in 5 - 30% of patients.
- Pre-med with benzos.
What “other system” effect does ketamine have?
- PLT aggregation inhibition
What are ketamine’s most common drug interactions?
- Volatiles → hypotension
- Non-depolarizing NMBs → enhancement
- Succinylcholine → prolongation
Why does ketamine prolong succinylcholine’s effects?
Ketamine is a plasma cholinesterase inhibitor.
Which induction agent has the highest analgesic properties?
- Ketamine
Why would ketamine be a decent induction drug for an OSA patient? Why not?
- Preservation of upper airway reflexes & ventilatory function.
- Sialagogue.
